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血红蛋白血症型钩端螺旋体病的发病机制与红细胞破坏

Pathogenesis and red blood cell destruction in haemoglobinaemic leptospirosis.

作者信息

Thompson J C, Manktelow B W

出版信息

J Comp Pathol. 1986 Sep;96(5):529-40. doi: 10.1016/0021-9975(86)90073-3.

DOI:10.1016/0021-9975(86)90073-3
PMID:3760265
Abstract

Sequential morphological changes were seen in RBCs, spleen and liver from hamsters during the development of haemoglobinaemia following infection with Leptospira interrogans serovar ballum. Spleens from pre-haemoglobinaemic hamsters showed sequestration of RBCs and erythrophagocytosis but to a lesser degree than was seen in the haemoglobinaemic hamsters. Erythrophagocytosis and RBC sequestration were also seen in the liver, particularly in the haemoglobinaemic animals. None of these changes was seen in the RBCs, spleens and livers from moribund and dead hamsters suffering from non-haemoglobinaemic disease resulting from infection with Leptospira interrogans serovar pomona. Intracellular leptospires were readily identifiable within the spleens and livers of hamster infected with both ballum and pomona. It is suggested that leptospiral toxins affect RBC metabolism and eventually RBC morphology. The affected cells are detected and removed by the reticulo-macrophage system, usually before intravascular haemolysis can take place. If the toxins affect a certain enzyme or biochemical pathway, there are sufficient normal metabolic differences in RBCs between animals of different species and, in the same species of animal, between the same and different aged animals, to explain the differing susceptibilities of the RBCs to leptospiral toxins.

摘要

在用问号钩端螺旋体巴姆血清型感染后血红蛋白血症发展过程中,仓鼠的红细胞、脾脏和肝脏出现了一系列形态学变化。血红蛋白血症前期仓鼠的脾脏显示有红细胞滞留和红细胞吞噬现象,但程度低于血红蛋白血症仓鼠。肝脏中也可见红细胞吞噬和红细胞滞留,尤其是在血红蛋白血症动物中。在用问号钩端螺旋体波摩那血清型感染导致的非血红蛋白血症疾病濒死和死亡的仓鼠的红细胞、脾脏和肝脏中未观察到这些变化。在感染巴姆和波摩那的仓鼠的脾脏和肝脏中很容易识别出细胞内钩端螺旋体。提示钩端螺旋体毒素影响红细胞代谢并最终影响红细胞形态。受影响的细胞通常在血管内溶血发生之前就被网状巨噬细胞系统检测并清除。如果毒素影响某种酶或生化途径,不同物种动物之间以及同一物种动物中相同年龄和不同年龄动物之间的红细胞存在足够的正常代谢差异,以解释红细胞对钩端螺旋体毒素的不同易感性。

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Infect Immun. 2002 Jan;70(1):315-22. doi: 10.1128/IAI.70.1.315-322.2002.
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